Pruritus Clinical Trial
Official title:
Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission
The following is the investigators hypothesis regarding the pruritus of BP patients during remission. Anti-BP 180 IgE binds to dermal mast cells, inducing their activation and secretion of mediators after being cross-linked by antigens. Among mediators, histamine directly induces itching and vessel changes, whereas tryptase potentiates itching and vessel changes in an indirect way through the actions of neuropeptides. Tryptase stimulates neurons which in turn secrete neuropeptides.
Bullous pemphigoid(BP) is a cutaneous autoimmune blister disease. In addition to blisters
formation which disrupt skin barrier and result in high mortality, erythematous edematous
plaques often develop on skin of bullous pemphigoid patients accompanied with intensive
pruritus. As regard with the pathogenesis of BP, it is generally accepted that anti-BP180
IgG is the most important pathogenic factor for blister formation, whereas anti-BP180 IgE
which binds to mast cells and induces their activation results in erythematous edematous
plaques. Quite a few bullous pemphigoid patients suffer from intensive pruritus even during
clinical remission period that means blisters or plaques are no longer on their skin. The
reasons why pruritus persists during this period are still obscure.
Pruritus is the most common symptom of cutaneous diseases. Our understanding regarding
pathophysiology of "pruritus" has made a remarkable progress in the past decade. Now, it is
known that there are various kinds of substances that induce pruritus (pruritus mediators)
and different combinations of these mediators are involved in different itching diseases.
Moreover, neuropeptides secreted by stimulated neurons can in turn induce neurogenic
inflammation.
The following is our hypothesis regarding the pruritus of BP patients during remission.
Anti-BP 180 IgE binds to dermal mast cells, inducing their activation and secretion of
mediators after being cross-linked by antigens. Among mediators, histamine directly induces
itching and vessel changes, whereas tryptase potentiates itching and vessel changes in an
indirect way through the actions of neuropeptides. Tryptase stimulates neurons which in turn
secrete neuropeptides.
Thus, in order to test our hypothesis, the strategy of this study is to compare parameters
between two groups of patients, bullous pemphigoid patients in remission with pruritus and
without pruritus. The following parameters in serum and skin will be measured: total IgE,
anti-BP 180 IgE, the number and activated status of mast cells, the amount of some mediators
and neuropeptides produced by mast cells and neurons, respectively. In addition, these
parameters in active stage will also be measured for reference and with a hope to find
useful parameters for predicting the persistence of pruritus in remission.
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Observational Model: Case Control, Time Perspective: Prospective
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